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Biomedical subjects

M C Kew

Publications and source records attributed to M C Kew.

At least 73 records · Page 4Linked to original sources
PubMed1991

Hypoglycemia in hepatocellular carcinoma: failure of short-term growth hormone administration to reduce enhanced glucose requirements.

The mechanism of tumor-associated hypoglycemia was investigated in 10 (six hypoglycemic and four normoglycemic) southern African blacks with hepatocellular carcinoma. The mean basal blood glucose concentration was significantly lower (2.4 +/- 0.1 v 3.6 +/- 0.2 mmol/L; P less than .01) and steady-state exogenous glucose requirements were increased fourfold (3.6 +/- 0.6 v 0.97 +/- 0.2 mg/kg/min; P less than .01) in the hypoglycemic compared with the normoglycemic patients. Plasma insulin and C-peptide levels were suppressed to the lower limit of sensitivity of each of the assays in both groups of patients. The concentrations of insulin-like growth factors (IGF) I and II were lower (19 +/- 1.6 v 25 +/- 4.6 insulin-like growth factors (IGF) I and II were lower (19 +/- 1.6 v 25 +/- 4.6 ng/L) and higher (230 +/- 42 v 173 +/- 40 ng/L), respectively, in the hypoglycemic patients, although the differences were not statistically significant. Of the counterregulatory hormones measured, only the growth hormone (GH) concentration was significantly lower in the hypoglycemic patients (0.9 +/- 0.2 v 18.6 +/- 5.6 micrograms/L; P less than .01). Correction of the plasma GH level into the high-normal physiological range in two hypoglycemic patients failed to reduce steady-state exogenous glucose requirements. However, the glucose requirements were reduced from 2.6 to 1.1 mg/kg/min in the same two patients when "acromegalic" plasma concentrations of GH were achieved. We conclude that steady-state glucose requirements are increased in black patients with hypoglycemia complicating hepatocellular carcinoma, and that short-term correction of the associated hyposomatotropism fails to reduce the enhanced requirements.

Blood Glucose↗
PubMed1991

Virchow-Troisier's lymph node in hepatocellular carcinoma.

Virchow-Troisier's lymph node is rarely found in patients with hepatocellular carcinoma. When present, it may or may not accompany spread of the tumor to mediastinal lymph nodes. In a 20-year-old South African black man with hepatocellular carcinoma, a Virchow-Troisier's node was evident clinically and confirmed at necropsy. Mediastinal lymph nodes were not involved by tumor, and the malignant cells probably gained access to the thoracic duct by way of lymphatic spread to the hepatic lymph nodes in the porta hepatitis and the celiac nodes, both of which were seen at necropsy to be extensively invaded by tumor.

Adult↗
PubMed1991

Rupture of hepatocellular carcinoma as a result of blunt abdominal trauma.

Spontaneous rupture of hepatocellular carcinoma occurs frequently in populations in which this tumor is common, but rarely in populations with a low incidence of the tumor. Rupture caused by blunt abdominal trauma has previously been reported in a single patient only. We describe three southern African black men who presented with an acute hemoperitoneum after blunt trauma to the abdomen, and in whom a moderate-size hepatocellular carcinoma was found at laparotomy to have ruptured. In two of the patients, it was possible to resect the tumor. This resectability rate is unusual in blacks with hepatocellular carcinoma, because the tumor is characteristically far advanced at the time of presentation and is rarely amenable to resection.

Abdominal Injuries↗
PubMed1990

Evaluation of CA 125 as a serum marker of hepatocellular carcinoma.

Serum CA 125 concentrations were raised in 90.4% of 115 southern African black patients with hepatocellular carcinoma. Seventy-four percent of 62 patients with amebic hepatic abscess, 60% of 40 patients with chronic hepatic parenchymal disease (chronic hepatitis or cirrhosis), and 60.9% of 41 patients with acute viral hepatitis also had raised values. The median serum CA 125 concentration for patients with hepatocellular carcinoma differed significantly from the benign hepatic disease groups analysed (p less than 0.0002). Serum alpha-fetoprotein levels were raised in 90.4% of the 115 hepatocellular carcinoma patients. CA 125 is thus a highly sensitive marker for hepatocellular carcinoma, but lacks specificity.

Acute Disease↗
PubMed1990

Hepatitis C virus antibodies in southern African blacks with hepatocellular carcinoma.

380 southern African blacks with hepatocellular carcinoma and 152 controls were studied. Antibodies to hepatitis C virus (HCV) were found in 110 patients and 1 control. 184 patients had evidence of current infection with hepatitis B virus (HBV) and 122 had had infection with this virus in the past. Only 47 patients had no markers of HCV or HBV infection. Among patients positive for HCV, there was a higher proportion of women and urban dwellers, and the average age was higher. In southern Africa, HCV is associated with hepatocellular carcinoma but HBV is present in a higher proportion of patients.

Adolescent↗
PubMed1990

Contraceptive steroids as a risk factor for hepatocellular carcinoma: a case/control study in South African black women.

The role of contraceptive steroids in the etiology or pathogenesis of hepatocellular carcinoma in urban South African black women was investigated in a hospital-based case and control study. Participating were 46 women, 19 to 54 yr old, with carcinoma, and 92 matched controls. South African blacks have a high incidence of hepatocellular carcinoma, and urban black women have used contraceptive steroids fairly widely for a number of years. Use of contraceptive steroids for longer than 6 mo (mean duration 46.7 mo) was not found to pose a risk for development of hepatocellular carcinoma in this population--relative risk 0.8 (95% confidence interval [C.I.] 0.4 to 1.7). This was also true of use for longer than 8 yr--relative risk 0.6 (95% C.I. 0.2 to 2.5), and if a combination of an estrogen and a progestogen or a progestogen alone was used (relative risk 1.7 [95% C.I. 0.7 to 4.2] and 0.4 [95% C.I. 0.1 to 1.2], respectively). Chronic hepatitis B virus infection was confirmed to have an etiological association with hepatocellular carcinoma, but there was no evidence that contraceptive steroids acted as a co-carcinogen with the virus or, conversely, that they played a causal role in patients negative for hepatitis B surface antigenemia. We cannot, however, exclude the possibility that contraceptive steroids may play a causal role in hepatocellular carcinoma in black women who have never been infected with the hepatitis B virus. Nor was there evidence that contraceptive steroids acted in concert with either cigarette smoking or chronic alcohol abuse in hepatocarcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Tumor hypoglycemia: relationship to high molecular weight insulin-like growth factor-II.

The mechanism of tumor-associated hypoglycemia was examined in 11 patients with hepatocellular carcinoma, 6 of whom presented with severe hypoglycemia and 5 in whom plasma glucose was persistently normal. Serum insulin levels in the hypoglycemic patients were low. Although total serum insulin-like growth factor II (IGF-II) levels in both groups of tumor patients were lower than normal, tumor tissue from hypoglycemic patients contained levels of IGF-II mRNA that were 10-20-fold higher than those present in normal liver. IGF-II immunoreactivity consisted in all cases of a mixture of both higher molecular weight forms and material having the character of IGF-II itself. The former comprised a greater proportion of total IGF-II, in patients with hypoglycemia. Studies to characterize the interactions of IGF-II with serum proteins showed that (a) the radiolabeled peptide bound to an approximately 40,000-D protein in sera from both hypoglycemic patients and normal subjects, (b) sera from hypoglycemic patients and normal subjects had similar capacity to bind the radiolabeled peptide, and (c) the apparent affinities of serum binding proteins for IGF-II were the same for both hypoglycemic patients and normal subjects. Whereas, acid extracted, tumor-derived IGF-II immunoreactive peptides with low or intermediate molecular weights bound to serum proteins in a manner indistinguishable from that of IGF-II itself, the highest molecular weight IGF-II immunoreactive peptide exhibited negligible ability to compete for radiolabeled ligand binding to serum proteins. The low affinity of serum binding proteins for this component suggests that high molecular weight IGF-II immunoreactivity might circulate free and be available for interaction with cell-surface receptors.

Adolescent↗
PubMed1989

The use of a monoclonal antibody against alpha-fetoprotein for the radioimmunodetection of hepatocellular carcinoma.

The purpose of this study was to investigate the use of a radiolabeled mouse monoclonal antibody (and its F(ab')2 fragment) against alpha-fetoprotein in the scintigraphic diagnosis of hepatocellular carcinoma. Twenty-six southern African Blacks and one Caucasian with hepatocellular carcinoma and four patients with other malignant tumors of the liver were studied. Although six hepatocellular carcinomas appeared to selectively concentrate alpha-fetoprotein antibody, one of these tumors was not producing alpha-fetoprotein. Moreover, in another 18 patients with alpha-fetoprotein-producing hepatocellular carcinomas, uptake of alpha-fetoprotein antibody was at best only equal to that in nontumorous hepatic tissue, and three hepatocellular carcinomas that were not producing alpha-fetoprotein concentrated the antibody to the same extent as did the alpha-fetoprotein-producing tumors and hepatic tissue. All four tumors other than hepatocellular carcinoma concentrated alpha-fetoprotein antibody as well as did hepatic tissue. These findings suggest that the penetration of hepatocellular carcinomas by alpha-fetoprotein antibody is a passive and nonselective process. This conclusion is supported by an in vitro study in which a non-alpha-fetoprotein-producing hepatic metastasis took up as much radiolabeled alpha-fetoprotein antibody as did three of four alpha-fetoprotein-producing hepatocellular carcinomas. A likely explanation for the failure of alpha-fetoprotein monoclonal antibody to be selectively concentrated by hepatocellular carcinomas is that alpha-fetoprotein is an export protein and is not expressed on the cell membranes of malignant hepatocytes.

Adult↗
PubMed1989

The role of membranous obstruction of the inferior vena cava in the etiology of hepatocellular carcinoma in Southern African blacks.

Membranous obstruction of the inferior vena cava has been incriminated as a risk factor for hepatocellular carcinoma in South African Blacks and in Japanese. However, the frequency with which this anomaly is found in patients with hepatocellular carcinoma, and hence its numerical importance as an etiological association of the tumor, has not been ascertained. Using radionuclide and contrast venography as well as necropsy and laparotomy examination, we investigated 162 unselected southern African Blacks with hepatocellular carcinoma together with appropriate controls for the presence of membranous obstruction of the inferior vena cava. Membranous obstruction of the inferior vena cava was detected in six of 162 (3.7%) hepatocellular carcinoma patients, compared with one of 279 subjects (0.36% p = 0.011) dying a violent death, none of 55 patients (p = 0.169) with malignant disease other than hepatocellular carcinoma and eight of 150 patients (5.3%; p = 0.336) being investigated for conditions which might have been associated with membranous obstruction of the inferior vena cava. Six of the 15 individuals (40%) found to have membranous obstruction of the inferior vena cava had concomitant hepatocellular carcinoma, confirming that membranous obstruction of the inferior vena cava constitutes a risk factor for the development of the tumor. However, only a very small proportion of hepatocellular carcinoma patients have this abnormality, so that it is a minor causal association of the tumor only.(ABSTRACT TRUNCATED AT 250 WORDS)

Black People↗
PubMed1989

Hepatocellular carcinoma with and without cirrhosis. A comparison in southern African blacks.

Hepatocellular carcinoma and cirrhosis frequently coexist. In populations with a low incidence of hepatocellular carcinoma, the tumor often arises as a complication of long-standing symptomatic cirrhosis, which may be micronodular or macronodular and which is usually alcoholic in origin, and cirrhosis per se is the major etiologic association of the tumor. The relation between these two pathologic conditions in populations with a high incidence of hepatocellular carcinoma has not hitherto been analyzed. In this study the association was examined in 463 southern African black men with hepatocellular carcinoma. Cirrhosis, almost always macronodular and rarely showing features of alcholic toxicity, was present in 63.1% of the patients. No differences were found in the age structure, clinical features, hepatic function, serum alpha-fetoprotein concentrations, or hepatitis B virus status between patients with hepatocellular carcinoma with and without cirrhosis. Patients with cirrhosis survived slightly longer, but the difference was not biologically significant. It is concluded that the relation between hepatocellular carcinoma and cirrhosis in southern African blacks differs substantially from that in low incidence regions of the tumor.

Adolescent↗
PubMed1989

Liver cell dysplasia accompanying hepatocellular carcinoma in southern Africa. Differences between urban and rural populations.

Liver cell dysplasia (LCD) has been recognised for many years in association with hepatocellular carcinoma (HCC). The presence of LCD relates to cirrhosis, particularly macronodular, as well as HBsAg positivity in many countries. These relationships have not previously been recognised in southern Africa. This study of LCD in 160 rural and urban black patients with proven HCC records a significant difference between the prevalence of dysplasia in rural HBsAg-positive and -negative cases: 75.6% in HBsAg+ individuals vs. 29.4% of those negative for HBsAg (P less than 0.01). Furthermore a significant relationship is reported between dysplasia and macronodular cirrhosis, LCD being observed in 62.9% of those with macronodular cirrhosis vs. 29.5% of non-cirrhotics (P less than 0.001). In addition there was evidence for a relationship between severity of dysplasia and domicile (rural greater than urban), age (being more extensive in younger patients), and ongoing viral replication (82.3% of patients showing the highest grade of dysplasia were found to be serum HBeAg+ and/or tissue HBcAg+ cf. 3.7% with absent or low-grade dysplasia). It is apparent that in southern Africa the presence of dysplasia in HBsAg+ individuals implies that HCC should be actively excluded in these patients and that they should thereafter be carefully monitored for the development of a tumour.

Adult↗
PubMed1989

Alpha-L-fucosidase as a serum marker of hepatocellular carcinoma in southern African blacks.

The purpose of this study was to compare alpha-L-fucosidase and alpha-fetoprotein as serum markers of hepatocellular carcinoma in 72 southern African blacks with this tumour and 64 matched patients with benign hepatic diseases which might be mistaken clinically for hepatocellular carcinoma. Alpha-L-fucosidase activity was assayed using p-nitrophenyl-L-fucopyranoside (pNpf) as a substrate and alpha-fetoprotein concentrations were measured by radioimmunoassay. Serum alpha-L-fucosidase activity in the patients with hepatocellular carcinoma (mean 1,268, s.e.m. +/- 83.7, median 1,150 and range 38-3,698 nmol pNpf ml-1 h-1) was significantly higher than that in the matched controls (mean 798, s.e.m. +/- 65.8, median 648 and range 273-3,825 nmol pNpf ml-1 h-1) (P = 0.0001). However, alpha-L-fucosidase was both less sensitive (75 versus 87%) and less specific (70 versus 87%) than alpha-fetoprotein as a serum marker of hepatocellular carcinoma. When, in an endeavour to eliminate false-positive results, the diagnostic cut-off level for alpha-L-fucosidase was increased to 1,500 nmol pNpf ml-1 h-1 and for alpha-fetoprotein to 400 ng ml-1, the sensitivity of alpha-L-fucosidase fell to 21% whereas that of alpha-fetoprotein remained satisfactory at 78%. If the two markers were used together, the number of false-negative alpha-fetoprotein results was reduced from 13 to 5.5%. We conclude that alpha-L-fucosidase is less useful than alpha-fetoprotein as a single marker of hepatocellular carcinoma in southern African blacks. However, the two markers can profitably be used together.

Africa, Southern↗
PubMed1989

Pityriasis rotunda as a cutaneous marker of hepatocellular carcinoma: a comparison with its prevalence in other diseases.

In an attempt to substantiate the claim that pityriasis rotunda may be a useful cutaneous marker of hepatocellular carcinoma in South African Blacks, the prevalence of the rash in 63 unselected South African Blacks with this tumour was compared to that in 63 matched patients with active tuberculosis, 63 with other malignant tumours, and 63 with various forms of chronic benign hepatic disease. The prevalence of pityriasis rotunda in hepatocellular carcinoma was 15.9%, which was appreciably greater (P = 0.0005) than the overall prevalence of the rash (2.6%) in the controls. The prevalence was 4.8% for tuberculosis (P = 0.038), 0% for other malignant diseases (P = 0.0007), and 3.2% for chronic benign hepatic disease (P = 0.015). We conclude that the presence of pityriasis rotunda is a useful pointer to the diagnosis of hepatocellular carcinoma in South African Blacks.

Adult↗
PubMed1989

Hepatocellular carcinoma presenting with the superior mediastinal syndrome.

Two southern African black men with hepatocellular carcinoma are described in whom spread of the tumor to mediastinal lymph glands caused obstruction to the superior vena cava. Although necropsy studies have shown that hepatocellular carcinoma occasionally metastasizes to mediastinal lymph glands, presentation with the superior mediastinal syndrome has not hitherto been reported.

Carcinoma, Hepatocellular↗
PubMed1989

Arterial hypertension as a paraneoplastic phenomenon in hepatocellular carcinoma.

Three South African blacks with hepatocellular carcinoma and arterial hypertension are described. Plasma angiotensinogen (renin substrate) concentrations were increased eightfold to 10-fold in the two patients in whom these concentrations were measured. One of these two patients also showed a 34-fold rise in plasma inactive, active, and total renin concentrations, and an elevated plasma renin activity (2.73 ng.L-1.s-1 angiotensin l/mL/h). Inactive renin (prorenin) constituted 90% of the total plasma renin concentration. In the third patient only plasma renin activity was measured, and this was considerably raised (6.05 ng.L-1.s-1; angiotensin l/mL/h). Thus, the arterial hypertension that rarely complicates hepatocellular carcinoma may be caused either by a combination of eutopic synthesis of excessive quantities of angiotensinogen and ectopic production and secretion of active renin by malignant hepatocytes, or by eutopic production of angiotensinogen alone.

Adult↗
PubMed1988

The prevalence of variant alkaline phosphatase in hepatocellular carcinoma in southern African blacks.

The prevalence of variant alkaline phosphatase in the serum of 335 southern African blacks with hepatocellular carcinoma was determined using polyacrylamide gel electrophoresis. The isoenzyme was detected in 2% (seven of 335) of the patients: it could not be found in the serum of 300 matched, healthy individuals or in 56 patients with various benign hepatic diseases. Variant alkaline phosphatase is thus of little use as a diagnostic marker of hepatocellular carcinoma in southern African blacks. The reported prevalence of this isoenzyme in hepatocellular carcinoma ranges between 3% and 31%. Higher frequencies usually are recorded in populations with a low incidence of the tumor, and the lowest frequencies have been found in Chinese patients. Our finding of variant alkaline phosphatase in only 2% of another high incidence population fits this trend. Patients with tumors that secreted the variant isoenzyme had a significantly higher serum total alkaline phosphatase activity than those with tumors lacking this property.

Alkaline Phosphatase↗